Journal
ORAL MICROBIOLOGY AND IMMUNOLOGY
Volume 24, Issue 6, Pages 478-484Publisher
WILEY
DOI: 10.1111/j.1399-302X.2009.00545.x
Keywords
bone loss; fimbriae; inflammation; macrophages; P; gingivalis; periodontitis
Funding
- Japan Society for the Promotion of Science
- AUG High-Tech Research Center Project
- Scientific Research, Ministry of Education, Japan
- US PHS [DE015254, DE018292]
- National Institutes of Health
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [R01DE015254] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL &CRANIOFACIAL RESEARCH [R01DE018292] Funding Source: NIH RePORTER
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Introduction: The fimA-encoded fimbriae of the periodontal pathogen Porphyromonas gingivalis display genetic diversity. Type I fimbriated P. gingivalis (Pg-I) has been most widely studied at the molecular level, whereas Pg-II is the most frequent isolate from severe periodontitis. Methods: To investigate virulence differences between Types I and II fimbriae, we examined strains 33277 (Pg-I) and OMZ314 (Pg-II), reciprocal swap mutants (i.e. expressing the heterologous fimbrial type), and their respective FimA-deficient derivatives. These organisms were tested in a mouse periodontitis model and in interactions with mouse macrophages, a cell type that plays important roles in chronic infections. Results: Strain 33277 induced significantly more periodontal bone loss than OMZ314 and substitution of Type II fimbriae with Type I in OMZ314 resulted in a more virulent strain than the parent organism. However, the presence of Type II fimbriae was associated with increased proinflammatory and invasive activities in macrophages. Conclusion: The inverse relationship between proinflammatory potential and ability to cause experimental periodontitis may suggest that an aggressive phenotype could provoke a host response that would compromise the persistence of the pathogen.
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